Red blood cell partitioning and blood flux redistribution in microvascular bifurcation

AbstractThis paper studies red blood cell (RBC) partitioning and blood flux redistribution in microvascular bifurcation by immersed boundary and lattice Boltzmann method. The effects of the initial position of RBC at low Reynolds number regime on the RBC deformation, RBC partitioning, blood flux redistribution and pressure distribution are discussed in detail. It is shown that the blood flux in the daughter branches and the initial position of RBC are important for RBC partitioning. RBC tends to enter the higher-flux-rate branch if the initial position of RBC is near the center of the mother vessel. The RBC may enter the lower-flux-rate branch if it is located near the wall of mother vessel on the lower-flux-rate branch side. Moreover, the blood flux is redistributed when an RBC presents in the daughter branch. Such redistribution is caused by the pressure distribution and reduces the superiority of RBC entering the same branch. The results obtained in the present work may provide a physical insight into the understanding of RBC partitioning and blood flux redistribution in microvascular bifurcation

Ion Migration Controlled Stability in α‑Particle Response of CsPbBr2.4Cl0.6 Detectors

Halide perovskites have been considered as nuclear radiation detection materials due to their high mobility, long carrier lifetime, and high absorption coefficient. However, it has been reported that the ion migration increases the dark current of halide perovskite detectors and hinders the stable response to high energy photons or particles. In this work, we report the utilization of the “voltage cycling” technique to obtain the stable α-particle spectra in a CsPbBr2.4Cl0.6 device. Also, by measuring the time-dependent stability and the effect of electric field strength, we can gain insight into the phenomona causing instability in these devices. Accordingly, the influence of ion migration on the charge transport properties and energy spectra in CsPbBr2.4Cl0.6 detectors was also revealed. Our investigation demonstrates the strong correlation between ion migration processes and stable energy spectra in halide perovskite materials

Solution-Grown Formamidinium Hybrid Perovskite (FAPbBr3) Single Crystals for α‑Particle and γ‑Ray Detection at Room Temperature

Compared with the widely reported MAPbBr3 single crystals, formamidinium-based (FA-based) hybrid perovskites FAPbBr3 (FPB) with superior chemical and structure stability are expected to be more efficient and perform as more reliable radiation detectors at room temperature. Here, we employ an improved inverse temperature crystallization method to grow FPB bulk single crystals, where issues associated with the retrograde solubility behavior are resolved. A crystal growth phase diagram has been proposed, and accordingly, growth parameters are optimized to avoid the formation of NH4Pb2Br5 secondary phase. The resulting FPB crystals exhibit a high resistivity of 2.8 × 109 Ω·cm and high electron and hole mobility–lifetime products (μτ) of 8.0 × 10–4 and 1.1 × 10–3 cm2·V–1, respectively. Simultaneously, the electron and hole mobilities (μ) are evaluated to be 22.2 and 66.1 cm2·V–1·s–1, respectively, based on the time-of-flight technique. Furthermore, a Au/FPB SC/Au detector is constructed that demonstrates a resolvable gamma peak from 59.5 keV 241Am γ-rays at room temperature for the first time. An energy resolution of 40.1% is obtained at 30 V by collecting the hole signals. These results demonstrate the great potential of FAPbBr3 as a hybrid material for γ-ray spectroscopy and imaging

Melt-grown large-sized Cs2TeI6 crystals for X-ray detection

Herein, we report the details of the synthesis and crystal growth of a lead-free perovskite derivative Cs2TeI6 crystal, which reveals long-term environmental stability. The synthesis process is optimized to obtain pure Cs2TeI6 polycrystals, and to eliminate the formation of residual CsI resulting from high vapor pressure. Subsequently, the Cs2TeI6 single crystal with dimensions of Φ10 mm × 55 mm is grown by the vertical Bridgman method. The as-grown 0-D structural Cs2TeI6 crystal exhibits a high resistivity of 9.92 × 1011 Ω cm, and resulting mobilities of 4.03 ± 0.33 cm2 V−1 s−1 and 9.40 ± 0.45 cm2 V−1 s−1 for electrons and holes, respectively. The Au/Cs2TeI6/Au device shows a good response for optoelectronic and X-ray detection, with a relatively high X-ray sensitivity of 27.8 μC Gy−1 cm−2 and a low detection limit of 72.5 nGy s−1

Towards superior X-ray detection performance of two-dimensional halide perovskite crystals by adjusting the anisotropic transport behavior

Two-dimensional (2D) organic–inorganic hybrid halide perovskites have recently attracted extensive attention for electronic and optoelectronic applications due to their tunable properties and superior stability compared with their three-dimensional (3D) counterparts. Here, we report two kinds of organic cation (linear butylamine (BA) and branched isobutylamine (i-BA)) tailored CsPbBr3 crystals, namely (BA)2CsPb2Br7 and (i-BA)2CsPb2Br7, grown by the temperature-cooling method. The organic cations' adjustable anisotropic structure, optoelectronic properties and X-ray detection performance have been systematically investigated. By shortening the spacer cation from BA to i-BA, the degree of anisotropy in 2D perovskite crystals is decreased, which may be ascribed to the reduced interlayer distance and barrier height resulting from the enhanced electronic coupling between neighboring organic cations. In particular, the device based on the (BA)2CsPb2Br7 crystal along the ab plane exhibits superior X-ray sensitivity up to 13.26 mC Gy−1 cm−2 at a relatively low electric field of 2.53 V mm−1, owing to the multiple quantum well structure that restricts the charge carrier transport within the ab plane resulting in efficient charge collection. Simultaneously, a superior long-term working stability is obtained under a high X-ray dose rate of 278.4 μGy s−1. We anticipate that these findings will be helpful for the development of Ruddlesden–Popper perovskites for future research and applications

The abnormal expression of circ-ARAP2 promotes ESCC progression through regulating miR-761/FOXM1 axis-mediated stemness and the endothelial–mesenchymal transition

Abstract Circular RNAs (circRNAs) belong to a novel class of noncoding RNA that gained more attention in human cancer pathogenesis. The role of circRNA in esophageal squamous cell carcinoma (ESCC) is largely unclear. Present investigation was to characterize new circRNAs regulating ESCC progression and explore the regulatory mechanisms in ESCC. In this study, circRNAs differentially expressed in ESCC and adjacent normal tissues were characterized via high-throughput sequencing. Then the differentially expressed circRNA between ESCC and adjacent normal tissues were investigated using Rt-qPCR. The role of circ-ARAP2 expression on tumor progression were detected in both in vivo and in vitro. Luciferase reporter assays were used to identify the relationships among circ-ARAP2, microRNA (miR)-761 and the cell cycle regulator Forkhead Box M1 (FOXM1). The result of the expression profile analyses regarding human circRNAs in ESCC demonstrated that circ-ARAP2 was up-regulated significantly in both ESCC tissues and cell lines. Downregulation circ-ARAP2 suppressed ESCC proliferation, tumor growth and metastasis in both in vivo and in vitro. The data also suggested that miR-761 and FOXM1 were circ-ARAP2 downstream targets which were confirmed through luciferase reporter analysis. Overexpression of FOXM1 or inhibiting miR-761 restored ESCC cell proliferation and invasion ability after silencing circ-ARAP2. The study also found that circ-ARAP2 influenced the endothelial–mesenchymal transition (EMT) and cancer stem cells differently by regulating miR-761/FOXM1. In one word, the results demonstrated that abnormal circ-ARAP2 expression promoted ESCC progression by regulating miR-761/FOXM1 axis-mediated stemness and EMT

DataSheet_2_Identification of NLE1/CDK1 axis as key regulator in the development and progression of non-small cell lung cancer.zip

Non-small cell lung cancer (NSCLC) is the most common pathological type of lung cancer, which is a severer threaten to human health because of its extremely high morbidity and mortality. In this study, the role of Notchless homolog 1 (NLE1) in the development of NSCLC was investigated and the underlying mechanism was explored. The outcomes showed that NLE1 expression is significantly higher in tumor tissues than normal tissues, and is correlated with the pathological stage. The regulation of NSCLC development by NLE1 was also visualized by the in vitro and in vivo loss-of-function studies, which indicated the inhibition of cell growth and migration, as well as enhancement of cell apoptosis on condition of NLE1 knockdown. As for the mechanism, it was demonstrated that NLE1 may execute its tumor-regulating function through activating E2F1-mediated transcription of CDK1, and PI3K/Akt signaling pathway was also supposed as a downstream of NLE1 in the regulation of NSCLC. Both CDK1 overexpression and treatment of Akt pathway activator could reverse the NLE1 knockdown induced NSCLC inhibition to some extent. In conclusion, this study identified NLE1 as a novel tumor promotor in the development and progression of NSCLC, which may be a potential therapeutic target in the treatment of NSCLC.</p

DataSheet_1_Identification of NLE1/CDK1 axis as key regulator in the development and progression of non-small cell lung cancer.zip

Non-small cell lung cancer (NSCLC) is the most common pathological type of lung cancer, which is a severer threaten to human health because of its extremely high morbidity and mortality. In this study, the role of Notchless homolog 1 (NLE1) in the development of NSCLC was investigated and the underlying mechanism was explored. The outcomes showed that NLE1 expression is significantly higher in tumor tissues than normal tissues, and is correlated with the pathological stage. The regulation of NSCLC development by NLE1 was also visualized by the in vitro and in vivo loss-of-function studies, which indicated the inhibition of cell growth and migration, as well as enhancement of cell apoptosis on condition of NLE1 knockdown. As for the mechanism, it was demonstrated that NLE1 may execute its tumor-regulating function through activating E2F1-mediated transcription of CDK1, and PI3K/Akt signaling pathway was also supposed as a downstream of NLE1 in the regulation of NSCLC. Both CDK1 overexpression and treatment of Akt pathway activator could reverse the NLE1 knockdown induced NSCLC inhibition to some extent. In conclusion, this study identified NLE1 as a novel tumor promotor in the development and progression of NSCLC, which may be a potential therapeutic target in the treatment of NSCLC.</p

Image_1_Identification of NLE1/CDK1 axis as key regulator in the development and progression of non-small cell lung cancer.pdf

Non-small cell lung cancer (NSCLC) is the most common pathological type of lung cancer, which is a severer threaten to human health because of its extremely high morbidity and mortality. In this study, the role of Notchless homolog 1 (NLE1) in the development of NSCLC was investigated and the underlying mechanism was explored. The outcomes showed that NLE1 expression is significantly higher in tumor tissues than normal tissues, and is correlated with the pathological stage. The regulation of NSCLC development by NLE1 was also visualized by the in vitro and in vivo loss-of-function studies, which indicated the inhibition of cell growth and migration, as well as enhancement of cell apoptosis on condition of NLE1 knockdown. As for the mechanism, it was demonstrated that NLE1 may execute its tumor-regulating function through activating E2F1-mediated transcription of CDK1, and PI3K/Akt signaling pathway was also supposed as a downstream of NLE1 in the regulation of NSCLC. Both CDK1 overexpression and treatment of Akt pathway activator could reverse the NLE1 knockdown induced NSCLC inhibition to some extent. In conclusion, this study identified NLE1 as a novel tumor promotor in the development and progression of NSCLC, which may be a potential therapeutic target in the treatment of NSCLC.</p